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Cotrimoxazole inhibits dhfr and dhps and reportedly selects for drug resistance in pathogens. Here,  Streptococcus mutans  isolates were obtained from saliva of HIV/AIDS patients taking cotrimoxazole prophylaxis in Uganda. The isolates were tested for resistance to cotrimoxazole and their  folP  DNA (which encodes sulfonamide-targeted enzyme dhps) cloned in pUC19. A set of recombinant plasmids carrying different point mutations in cloned folP were separately transformed into  folP -deficient  Escherichia coli . Using sulfonamide-containing media, we assessed the growth of  folP -deficient bacteria harbouring plasmids with differing  folP  point mutations. Interestingly, cloned  folP  with three mutations (A37V, N172D, R193Q) derived from  Streptococcus mutans  8 conferred substantial resistance against sulfonamide to  folP -deficient bacteria. Indeed, change of any of the three residues (A37V, N172D, and R193Q) in plasmid-encoded  folP  diminished the bacterial resistance to sulfonamide while removal of all three mutations abolished the resistance. In contrast, plasmids carrying four other mutations (A46V, E80K, Q122H, and S146G) in  folP  did not similarly confer any sulfonamide resistance to  folP -knockout bacteria. Nevertheless, sulfonamide resistance (MIC = 50   μ  M) of  folP -knockout bacteria transformed with plasmid-encoded  folP  was much less than the resistance (MIC = 4 mM) expressed by chromosomally-encoded  folP . Therefore,  folP  point mutations only partially explain bacterial resistance to sulfonamide.

Point Mutations in thefolPGene Partly Explain Sulfonamide Resistance ofStreptococcus mutans